MOTS-C
Mitochondrial-derived peptide, cellular energy metabolismA mitochondrial peptide protocol aimed at energy metabolism and training adaptation, screened against your baseline and monitored through the course.
Roughly 90% of your cellular energy comes from mitochondria, MOTS-C is a peptide your mitochondria produce themselves, acting as an exercise signal. Human evidence is early, and your consultant will be direct about what is and isn’t established. Full reference →
Who this is for
Adults with declining training capacity, energy, or metabolic markers, where labs support a mitochondrial indication. Candidacy is decided with your consultant against your history and baseline, never by a checkout flow.
How the program works
Your consultant goes through your goals, history, and whether this therapy is appropriate. If it isn't, you'll hear that instead.
An at-home blood draw establishes your metabolic baseline. Your pen ships cold-chain once your program is agreed.
Micro-doses on training days. Video review at week 6, messaging in between.
Labs and training data compared against baseline. Together you decide: continue, adjust, or stop with a plan.
Common questions
Some athletes report changes in endurance and recovery within weeks; for others it is gradual. Progress is read from your labs and training data at weeks 6 and 12 rather than promised.
No, the opposite. MOTS-C behaves like an exercise signal, so it works with training load, not instead of it. Your consultant will expect a structured program alongside it.
Your program is quoted in full after your consultation, before anything is supplied. There is no set program price because there is no off-the-shelf product: dose, schedule and monitoring differ per patient.
MOTS-c is named after its origin: a mitochondrial open reading frame within the 12S rRNA region of mitochondrial DNA. The -c denotes the specific peptide fragment characterized in the founding 2015 paper. It is a 16-amino-acid peptide encoded within the mitochondrial 12S ribosomal RNA region. Unlike all conventional signalling peptides which are encoded in the nuclear genome, MOTS-c is encoded in mitochondrial DNA, which makes it a member of the mitochondrial-derived peptide (MDP) class.
MOTS-c was first characterised in 2015 by Lee and colleagues in a landmark paper in Cell Metabolism (Lee C, Zeng J, Drew BG, et al. Cell Metab. 2015;21(3):443-454. PMID: 25738959). The discovery came from a systematic search of the mitochondrial genome for hidden open reading frames.
No. MOTS-c has no regulatory approval as a pharmaceutical in any jurisdiction. It is supplied as a research peptide for laboratory use only. The published evidence base is predominantly mouse models and in vitro mechanistic studies.
The Reynolds 2021 Nature Communications paper reported that exercise induces endogenous MOTS-c expression in human skeletal muscle, and that intermittent MOTS-c treatment in mice increased physical capacity and improved measures of healthspan. The combination of exercise-induced expression in humans and exogenous-administration effects in mice supports the framing of MOTS-c as an exercise-mimetic research compound. The framing remains a research hypothesis rather than a clinical claim.
A peptide written in mitochondrial DNA
MOTS-c regulates cellular metabolism in an AMPK-dependent manner. AMPK (AMP-activated protein kinase) is the master metabolic switch that responds to cellular energy state. The AMPK-dependent mechanism underpins the metabolic homeostasis effects reported in the Lee 2015 discovery paper.
Kim and colleagues (Cell Metab, 2018;28(3):516-524) reported that MOTS-c translocates to the nucleus in response to metabolic stress and regulates nuclear gene expression. The nuclear translocation provides a mechanism by which a mitochondrial-encoded peptide influences nuclear-genome gene expression.
Lee and colleagues (Cell Metab, 2015;21(3):443-454) reported that MOTS-c administration in mice promoted metabolic homeostasis and reduced obesity and insulin resistance in diet-induced obese models. The published findings provide the basis for insulin sensitivity research applications.
Reynolds and colleagues (Nat Commun, 2021;12:470) reported that exercise induces endogenous MOTS-c expression in human skeletal muscle and that intermittent MOTS-c treatment increased physical capacity in mouse models across multiple age groups. The work supports the "exercise mimetic" framing common in MOTS-c commentary.
MOTS C is also searched as MOTSC, Mitochondrial-derived peptide.